Association Between Blood Ammonia Level And Severity Of Portal Hypertensive Gastropathy in Egyptian patients with post Hepatitis C virus cirrhosis

Abstract

Cirrhosis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, characterized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. In most persons, approximately 80 to 90 percent of the liver parenchyma must be destroyed before liver failure is manifested clinically. When complications of cirrhosis occur, they typically are related to impaired hepatic function or actual physical disruption and re organization of the liver parenchyma. Portal hypertension is a frequent clinical syndrome caused by intrinsic liver disease, obstruction, or structural changes that result in increased portal blood flow or increased hepatic resistance. It characterized by a pathological increase in portal venous pressure and the formation of portosystemic collaterals that divert portal blood to the systemic circulation, by passing the liver. The increased portal pressure leads to an increase in the pressure gradient between the portal vein and the hepatic veins. Not all patients with an increased portal venous pressure should be considered as having clinical portal hypertension, because the complications of portal hypertension are observed only when the portal pressure gradient is increased above threshold value of about 12 mm Hg. This value therefore defines what is known as clinically significant portal hypertension. The importance of this syndrome is due to its frequency and to the severity of its complications.